The purpose of this investigation is to elucidate the mechanism by which glucocorticoids and estrogen accelerate fetal lung maturation and stimulate surfactant production. The experimental models which we will use are the pregnant rabbit and mouse. We will focus on the mechansim by which these hormones stimulate the activity of fetal lung cholinephosphate cytidylyltransferase. We will determine whether these hormones increase the molecular size of the enzyme and whether they alter its kinetic properties. We will determine whether the hormones act via phosphatidylglycerol or other acidic phospholipids. We will measure such lipid levels in the lung and also measure the activities of enzymes involved in their biosynthesis. We will also determine the mechanism by which estrogen and glucocorticoids deplete fetal lung glycogen. We will examine the effect of these hormones on glycogen synthase and glycogen phosphorylase. This work is important in understanding the mechanism by which hormones accelerate fetal lung maturation. Such information is essestial in order to prevent and possibly treat the respiratory distress syndrome which is a major cause of morbidity and mortality in premature infants in the United States and other developed countries.